Role of p38MAPK/eNOS signaling pathway in the inhibition of AGEs-induced apoptosis of human umbilical vein endothelial cells by glucagon-like peptide-1.
- Author:
Hailong ZENG
1
;
Zhiqiu HUANG
;
Yineng ZHANG
;
Huilin SUN
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; Cells, Cultured; Glucagon-Like Peptide 1; pharmacology; Glycation End Products, Advanced; metabolism; Human Umbilical Vein Endothelial Cells; cytology; metabolism; Humans; Nitric Oxide Synthase Type III; metabolism; Phosphorylation; Signal Transduction; p38 Mitogen-Activated Protein Kinases; metabolism
- From: Journal of Southern Medical University 2016;36(1):116-139
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of p38MAPK signaling pathway in the mechanism by which glucagon-like peptide-1 (GLP-1) inhibits endothelial cell damage induced by AGEs.
METHODSHuman umbilical vein endothelial cells were divided into control group, AGEs group, GLP-1 group, AGEs+GLP-1 group, AGEs+inhibitor group, and AGEs+GLP-1+inhibitor group. The expressions of p-p38MAPK/p38MAPK and p-eNOS/eNOS protein were examined by Western blotting, and the cell apoptosis rates were tested by flow cytometry.
RESULTSCompared with the control group, AGEs significantly enhanced the expression of p-p38 MAPK protein (P=0.001) while GLP-1 significantly inhibited its expression (P<0.001). AGEs significantly inhibited the expression of p-eNOS protein (P=0.007), which was enhanced by GLP-1 and p38 MAPK inhibitor (SB203580) (P=0.004). Both SB203580 and GLP-1 treatment decreased the apoptosis rate of AGEs-treated cells (P<0.001).
CONCLUSIONGLP-1 can protect human umbilical vein endothelial cells against AGEs-induced apoptosis partially by inhibiting the phosphorylation of p38MAPK protein and promoting the expression of p-eNOS protein.
